Biomedical subjects

Gyula Mózsik

Publications and source records attributed to Gyula Mózsik.

7 recordsLinked to original sources

PubMed2003

[Activation of the nuclear factor kappa B--key role in oncogenesis? Chronic hepatitis C virus infection and lymphomagenesis].

INTRODUCTION: Hepatitis C virus (HCV) infection may have an etiopathogenic role in development of B-cell non-Hodgkin lymphoma (NHL). Antiapoptotic effect of the HCV may display via activation of nuclear factor kappa B (NF-kappa B) transcription factor and can lead to development of carcinoma. AIMS: 1. Activated NF-kappa B was examined in peripheral blood lymphocytes of patients with HCV infection or NHL, and HCV positive B-cell NHL. 2. NF-kappa B was detected in liver biopsies of patients with HCV positive hepatocellular carcinoma (HCC) and in lymphnodes of patients with HCV positive NHL. PATIENTS AND METHODS: 1. Fifteen patients with chronic HCV infection, 13 patients with B-cell NHL (among them 4 HCV positive) and 10 healthy subjects were examined for the activity of NF-kappa B using electrophoretic mobility shift assay (EMSA). 2. Immunohistochemistry was performed in 8 liver biopsies from HCV positive patients and 2 HCC patients (1 HCV positive and 1 HCV negative) and 2 B-cell NHL patients (1 HCV positive and 1 HCV negative). RESULTS: 1. In the HCV negative control samples there was no shift detected, but we found NF-kappa B specific oligonucleotide-protein complexes in the lymphocyte extracts from all HCV positive patients and 10/13 (76.92%) in B-cell NHL. 2. NF-kappa B was detectable in 7/8 cases in liver biopsies from HCV positive patients. Strong reaction was detected in nuclei in HCV positive HCC and NHL patients (no reaction in HCV negative biopsies). CONCLUSIONS: NF-kappa B activation was justified in both diseases, which can connect the development of both HCV infection and B-cell NHL. This factor activation may have role in hepato- and lymphomagenesis.

Adult↗

PubMed2002

[Investigation of the gene locus in autosomal polycystic kidney disease in a 21 year old female patient with congenital hepatic fibrosis and polycystic liver].

BACKGROUND: Congenital hepatic fibrosis is an uncommon cause of portal hypertension in childhood or the early adolescence, usually presented with hepatomegaly and bleeding from esophageal varices. Despite the hepatomegaly and the fibrotic reconstruction of the liver the liver function tests are usually normal. In most cases it is associated with cystic disease of the kidneys. Congenital hepatic fibrosis is a constant feature of autosomal recessive polycystic kidney disease. CASE: The authors report on the case of a female patient with polycystic kidneys and polycystic liver. The symptoms of portal hypertension presented in the age of 20, on the basis of liver biopsy congenital hepatic fibrosis was diagnosed. AIMS: The authors intended to investigate whether there is genetic alteration as common etiology behind the rare association of congenital hepatic fibrosis confirmed in the adolescence and the polycystic disease of the liver and the kidneys. The clinical manifestation raised the possibility of autosomal recessive polycystic kidney disease. Segregation of microsatellite markers for autosomal recessive polycystic kidney disease gene locus 6p21.1-p12 was examined in the affected family to assess the possible role of theis gene. RESULTS: Four out of the 6 polymorphic microsatellite markers were informative, indicating that the autosomal recessive polycystic kidney disease may be responsible for the development of the rare association of the lesions of the liver and the kidneys in authors' patient.

Adult↗

PubMed2002

[Hepatitis C and immunoglobulin heavy-chain gene rearrangement].

UNLABELLED: Hepatitis C virus (HCV) has cytopathogenic effect not only on hepatocytes, however on salivary glands, monocytes of peripheral blood and lymphoid cells, may explain the systemic manifestations of the infection. HCV activates B and T-cells, modifies the immune response, causes lymphoproliferation, leading the development of B-cell non-Hodgkin's lymphoma (NHL). In the majority of B-cell NHLs immunoglobulin heavy chain (IgH) and light chain (IgL) genes are rearranged and expressed on cell surface in the early stage of the ontogenesis. The analyses of IgH rearrangement prove the clonality of lymphoproliferative disorders giving a powerful approach to the B-cell origin identification of cell proliferation. PATIENTS AND METHODS: IgH gene rearrangements were examined from the sera of 57 chronic HCV infected patients and 11 HCV-positive cryoglobulinemic patients as well. RESULTS: Cryoglobulinemia was detected in 20% of all chronic hepatitis C virus infected patients and IgH rearrangement was observed in 10.29% (7/68), 4/7 patients (57.14%) suffered from cryoglobulinemia. CONCLUSIONS: These results support the hypothesis that IgH gene rearrangement in HCV positive patients can indicate the lymphoproliferative disorder in the HCV infection released B-cell proliferation and lymphoma development.

Adult↗

PubMed2002

[Prevalence of Leiden mutation in various gastrointestinal disorders].

Molecular biological examinations have been carried out by the authors from 1995 in patients with different haemostasis, very recently these types of the studies were done in patients with different gastrointestinal (Helicobacter pylori-induced gastritis, hepatitis C infection, ileitis terminalis, ulcerative colitis, colon polyposis and adenocarcinoma in polyps) disorders. AIM, PATIENTS, METHOD: The Leiden mutation was detected by polymerase chain reaction (PCR) in 1354 healthy persons and patients with different GI disorders. RESULTS: The results of Leiden prevalence in patients with different gastrointestinal disorders were compared to those obtained in patients with venous thrombosis and familiar thrombophilia. The authors indicated that the prevalence of heterozygous Leiden positive persons was 5.9% in healthy (n = 87) and blood donors (n = 600). The prevalence of heterozygous Leiden mutation was 27% in patents who under went venous thrombosis (n = 300; P < 0.001), 38% in patients with familial thrombophilia (n = 116; P < 0.001). The prevalence of Leiden mutation was 0 in patients with Helicobacter pylori-induced gastritis (n = 24), 8% in hepatitis C infections (n = 75), 14.28% in Crohn's disease, (n = 49; P < 0.01), 27.5% in ulcerative colitis (n = 35; P < 0.001), 44% in colon polyposis (n = 59; P < 0.001) and 55% in situ adenocarcinomas (in polyposis) (n = 9; P < 0.001). CONCLUSION: The presented results suggest that the Leiden mutation is involved in patients with different inflammatory bowel disease, colon polyposis, as one of the suggested genetic factors.

Colonic Polyps↗

PubMed2002

[Gene therapy in liver diseases].

The basic principles of gene therapy, ex vivo and in vivo gene transfers and various vectors have been reviewed first in the paper. Then the models for clinical application are shown, including the recent results of experimental studies, with special regard to the treatment of liver diseases and amongst them hepatocellular carcinoma. Gene therapy is still in preclinical stage. Due to the ongoing intensive genetic studies and if the existing problems being resolved in this field, we can predict that the early years of this millennium gene therapy will be a useful modality in the clinical hepatology as well.

Animals↗

PubMed2002

[Genetic aspects of liver diseases].

Genetic factors play a privotal role in the pathogenesis of several liver diseases. A review is devoted to discussing the genetics of autoimmune hepatitis, chronic viral hepatitis B and C, cholestatic and alcoholic liver diseases, UDP-glucuronyl transferase deficiency, alpha, antitripsin deficiency, hereditary haemochromatosis, Wilson's disease and hepatocellular carcinoma.

Carcinoma, Hepatocellular↗

PubMed2002

Decrease in CD3-negative-CD8dim(+) and Vdelta2/Vgamma9 TcR+ peripheral blood lymphocyte counts, low perforin expression and the impairment of natural killer cell activity is associated with chronic hepatitis C virus infection.

BACKGROUND/AIMS: As chronic hepatitis C virus (HCV) infection is associated with impaired natural killer (NK) cell cytotoxicity, we examined the phenotypes and perforin expression of peripheral blood lymphocytes, as well as the effect of interferon-alpha2b (IFN-alpha2b) therapy. METHODS: Thirty-three patients had chronic hepatitis C, and of them 12 had been on IFN-alpha2b treatment. Eleven individuals had been treated earlier with IFN-alpha2b and completely cured, and eight were HCV carriers with persistently normal serum alanine aminotransferase. Three-colour flow cytometry was used to measure the percentage of CD3(+/-)CD8+, CD3+CD4+, gammadeltaTcR+, Vdelta2 TcR+, Vgamma9 TcR+, Vdelta1 TcR+, CD3-CD16+, CD3-CD56+, CD19+ and perforin-positive cells. NK cell activity was assessed by single cell cytotoxic and flow cytometric assay. RESULTS: Patients with chronic hepatitis C showed an impaired NK cytotoxicity, decreased percentage of CD3-negative-CD8dim-positive (NK subtype) and Vgamma9/Vdelta2 TcR+ as well as perforin-positive T lymphocytes, compared to controls and to those who were cured from HCV infection. IFN-alpha2b increased NK cell cytotoxicity and the percentage of perforin-positive lymphocytes. CONCLUSIONS: Our findings suggest that in chronic HCV infection a decreased percentage of CD3(-)CD8+, Vgamma9/Vdelta2 TcR+ and perforin-positive T cells and simultaneous decreased peripheral NK activity may contribute to the impaired cellular immune response and the chronicity of the disease.

Adult↗